The use of low concentrations of divalent cations to demonstrate a role for N-methyl-D-aspartate receptors in synaptic transmission in amphibian spinal cord.

Abstract:

:1 Synaptic potentials and the responses of frog spinal cord to various acidic amino acids were examined by means of the sucrose gap recording technique. 2 Divalent cations (50-250 microM) specifically antagonized responses evoked at N-methyl-D-aspartate (NMDA) receptors by N-methyl D,L aspartic acid (NMDLA). The rank order of potency was Ni2+ greater than Co2+ greater than Mg2+ greater than Mn2+. Responses to glutamate and aspartate were relatively insensitive to these concentrations of divalent cations. 3 The rank order of potency for divalent ions (1 mM) for antagonism of synaptic transmission in bullfrog sympathetic ganglia was Mn2+ greater than Co2+ greater than Ni2+ greater than Mg2+. Thus synaptic transmission in ganglia was especially sensitive to Mn2+ whereas NMDLA responses were especially sensitive to Co2+ and Mg2+. 4 It was possible to depress selectively the dorsal root-dorsal root potential (DR-DRP) and dorsal root-ventral root potential (DR-VRP) of frog spinal cord using low doses of Co2+ or Mg2+ which did not affect VR-DRP (ventral root-dorsal root potential). It was not possible to produce this selective depression of DR-DRP and DR-VRP with Mn2+, as this cation non-selectively depressed all responses. 5 These results suggest that: (i) divalent cations do not antagonize NMDLA responses by blocking Ca2+ channels which may mediate the response; (ii) postsynaptic NMDA receptors are activated by a neurotransmitter involved in the DR-DRP and DR-VRP pathways but not by any neurotransmitters involved in the VR-DRP pathway; (iii) the neurotransmitter activating NMDA receptors in amphibian spinal cord may be an aspartate-like substance rather than aspartate itself or glutamate.

journal_name

Br J Pharmacol

authors

Smith PA

doi

10.1111/j.1476-5381.1982.tb09306.x

subject

Has Abstract

pub_date

1982-10-01 00:00:00

pages

363-73

issue

2

eissn

0007-1188

issn

1476-5381

journal_volume

77

pub_type

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